Ask about this productRelated genes to: Galnt11 antibody
- Gene:
- GALNT11 NIH gene
- Name:
- polypeptide N-acetylgalactosaminyltransferase 11
- Previous symbol:
- -
- Synonyms:
- GalNAc-T11
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-28
- Date modifiied:
- 2015-08-27
Related products to: Galnt11 antibody
Related articles to: Galnt11 antibody
- Placental dysfunction and immune dysregulation are central to disorders such as fetal growth restriction (FGR) and preeclampsia (PE). Although aberrant placental glycosylation has been implicated in various pregnancy complications, the specific expression patterns of glycosylation-related genes (GRGs) associated with placental pathology and their potential role in driving immune imbalance at the maternal-fetal interface remain poorly understood. - Source: PubMed
Publication date: 2026/07/23
Yin TingxuanHu XianyangYu HailinZhang TianqiYu QinHuang XixiXu ChunfangTang ChuanlingLiu LuDu Meirong - The family of low-density lipoprotein receptor (LDLR) and LDLR-related proteins (LRPs) are endocytic receptors serving as essential regulators of multiple physiological processes including cholesterol clearance, protein reabsorption, and neuronal protein trafficking. Site-specific O-glycans modify linkers of the ligand-binding domains of LRPs. Most linker O-glycans are initiated exclusively by GALNT11, 1 of 20 polypeptide GalNAc-transferase isoenzymes. Here, we investigate the role of GALNT11 linker O-glycans in the large and widely expressed multiligand receptor LRP1. In cell models expressing LRP1 with and without GALNT11, we demonstrate that while the uptake of certain ligands such as RAP and ApoE was unaffected, uptake of neurotoxic tau and amyloid-β was altered and in opposite directions. Characterization of LRP1 linker O-glycans indicated incomplete sialic acid capping, a feature that, in MD simulations, enabled inter- and intramolecular interactions. Our findings highlight a potential regulatory mechanism of endocytic receptors and identify the ligand repertoire of LRP1 as influenced by O-glycans, with implications for neurodegenerative disease. - Source: PubMed
Publication date: 2026/06/05
Hintze JohnTopaktas Asli BMadsen Thomas DJebari-Benslaiman ShifaClaridge Bethany HD'Andrea Silviade Haan NoortjeHansen Lasse HBaars RobQuittot NoéMartin CesarYang ZhangVakhrushev Sergey YMiller Rebecca LStrickland Dudley KHyman BradleyFadda ElisaSchjoldager Katrine T - We investigated the genetic determinants of variation in the hemoglobin glycation index (HGI), an emerging biomarker for the risk of diabetes complications. - Source: PubMed
Publication date: 2024/10/28
House John SBreeyear Joseph HAkhtari Farida SEvans VioletBuse John BHempe JamesDoria AlessandroMychaleckyi Josyf CFonseca VivianShi MengyaoLi ChangweiLiu ShuqianKelly Tanika NRotroff DanielMotsinger-Reif Alison A - Genomic profiling has revolutionized therapeutic interventions and the clinical management of liver cancer. However, pathogenetic mechanisms, molecular determinants of recurrence, and predictive biomarkers for first-line treatment (anti-PD-(L)1 plus bevacizumab) in liver cancer remain incompletely understood. Targeted next-generation sequencing (tNGS) (a 603-cancer-gene panel) was applied for the genomic profiling of 232 hepatocellular carcinoma (HCC) and 22 intrahepatic cholangiocarcinoma (ICC) patients, among which 47 unresectable/metastatic HCC patients underwent anti-PD-1 plus bevacizumab therapy. Genomic alterations were estimated for their association with vascular invasion (VI), location of onset, recurrence, overall survival (OS), recurrence-free survival (RFS), and anti-PD-1 plus bevacizumab therapy response. The genomic landscape exhibited that the most commonly altered genes in HCC were , , , , , and , while , , , , , and were frequently altered in ICC; notably, (18.18% vs. 1.29%) and (13.64% vs. 1.29%) alterations were significantly more prevalent in ICC. Comparison analysis demonstrated the distinct clinicopathological/genomic characterizations between Chinese and Western HCC cohorts. Genomic profiling of HCC underlying VI showed that , , , , and were frequently altered in the VI group compared to patients without VIs. Compared to the right hepatic lobes of HCC patients, the left hepatic lobe of HCC patients had superior OS (median OS: 36.77 months vs. unreached, < 0.05). By further comparison, Notch signaling pathway-related alterations were significantly prevalent among the right hepatic lobes of HCC patients. Of note, multivariate Cox regression analysis showed that altered , , , , and , as independent prognostic factors, were significantly correlated with the OS of HCC patients. Furthermore, altered was abundantly enriched in the HCC-recurrent group, and impressively, it was independent of clinicopathological features in predicting RFS (median RFS of altered type vs. wild-type: 5.57 months vs. 22.47 months, < 0.01). Regarding those treated HCC patients, TMB value, altered , and cell cycle-related alterations were identified to be positively associated with the objective response rate (ORR), but alterations were negatively correlated with ORR. In addition, altered and cell cycle signaling were significantly associated with reduced and increased time to progression-free survival (PFS), respectively. Comprehensive genomic profiling deciphered distinct molecular characterizations underlying VI, location of onset, recurrence, and survival time in liver cancer. The identification of novel genetic predictors of response to anti-PD-1 plus bevacizumab in HCC facilitated the development of an evidence-based approach to therapy. - Source: PubMed
Publication date: 2024/06/14
Wang YizhouShang PeipeiXu ChangDong WeiZhang XiaofengXia YongSui ChengjunYang Cheng - O-glycosylation is a conserved posttranslational modification that impacts many aspects of organismal viability and function. Recent studies examining the glycosyltransferase Galnt11 demonstrated that it glycosylates the endocytic receptor megalin in the kidneys, enabling proper binding and reabsorption of ligands, including vitamin D-binding protein (DBP). Galnt11-deficient mice were unable to properly reabsorb DBP from the urine. Vitamin D plays an essential role in mineral homeostasis and its deficiency is associated with bone diseases such as rickets, osteomalacia, and osteoporosis. We therefore set out to examine the effects of the loss of Galnt11 on vitamin D homeostasis and bone composition. We found significantly decreased levels of serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, consistent with decreased reabsorption of DBP. This was accompanied by a significant reduction in blood calcium levels and a physiologic increase in parathyroid hormone (PTH) in Galnt11-deficient mice. Bones in Galnt11-deficient mice were smaller and displayed a decrease in cortical bone accompanied by an increase in trabecular bone and an increase in a marker of bone formation, consistent with PTH-mediated effects on bone. These results support a unified model for the role of Galnt11 in bone and mineral homeostasis, wherein loss of Galnt11 leads to decreased reabsorption of DBP by megalin, resulting in a cascade of disrupted mineral and bone homeostasis including decreased circulating vitamin D and calcium levels, a physiological increase in PTH, an overall loss of cortical bone, and an increase in trabecular bone. Our study elucidates how defects in O-glycosylation can influence vitamin D and mineral homeostasis and the integrity of the skeletal system. - Source: PubMed
Publication date: 2024/03/12
Tian ERothermel CarolineMichel Zacharyde Castro Luis FernandezLee JeeyoungKilts TinaKent TristanCollins Michael TTen Hagen Kelly G